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Mindy Engevik PhD

Mindy Melinda A Engevik PhD

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  • Assistant Professor
  • College of Medicine
  • Regenerative Medicine and Cell Biology
Academic Focus
  • Microbe-mucus interactions
  • Pathogen-host interactions
  • Intestinal Wound healing
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Our recent understanding of the gut microbiota has sparked interest in investigating microbes’ ability to colonize and modulate the gut environment. The intestinal mucus layer serves as the first point of contact between the gut microbiota and the host. In addition to providing a barrier for the epithelium, the mucus layer provides a niche for bacteria due to its abundance of attachment sites and potential as a nutrient source. Dr. Mindy Engevik’s lab investigates microbial-host crosstalk with an emphasis on microbe-mucus interactions.

The Engevik lab has 2 main focuses: (1) how commensal microbes beneficially modulate the mucus layer and host health; and (2) how pathogens colonize and subvert the mucus layer to cause infection.

(1) One of our favorite commensal microbes is Bifidobacterium dentium. We have identified that B. dentium metabolites stimulate the release of serotonin from intestinal enterochromaffin cells. Serotonin activates up to 14 different intestinal serotonin receptor subtypes, including ones on mucus-producing goblet cells. We hypothesize that serotonin activates goblet cell 5-HTR4, stimulating the release of mucus and the healing peptide trefoil factor (TFF3). Our preliminary data with human intestinal organoid, also known as enteroid, monolayers indicates that serotonin and B. dentium metabolites enhance wound healing. So now we need to dissect the mechanisms, identify candidate metabolites, examine these effects in vivo and more! Ultimately, these studies could provide new targets for promoting epithelial repair and wound healing.
Working model of how commensal microbes beneficially modulate the mucus layer and host health
(2) In terms of pathogens, we also study Clostridium difficile. C. difficile which is the most common healthcare associated pathogen in U.S. hospitals, incurring billions of dollars in treatment costs each year. Studies have shown that antibiotic disruption of the gut microbiota creates a favorable niche for C. difficile spore germination and ultimately toxin production and disease. Our previous work has demonstrated that C. difficile adheres to intestinal mucus with mucin-degrading bacteria such as Bacteroides, Ruminococcus, and Akkermansia. We also identified a high abundance of Fusobacterium, an oral microbe known to form multi-species biofilms. We now want to know how Fusobacterium and these other microbes influences C. difficile infection. These studies will characterize microbe-microbe signaling networks involved in C. difficile infection.
Working model of how pathogens colonize and subvert the mucus layer to cause infection